Tobacco use is one of the most potent avoidable causes for cardiovascular (C-V) disease. Epidemiologic studies indicate that even small amounts of secondhand smoke (SHS) exposure increase C-V disease risk. However, the long-term effect of childhood SHS exposure on the life course C-V disease risk is not clear. Importantly, data on dose-response relationship, interaction of SHS with C-V risk factors and racial (black-white) divergence are limited. The proposed research is designed to test the hypothesis that childhood SHS exposure and its impact on C-V disease risk from childhood to adulthood vary by race within a black-white population. In response to the FOA (PA-11-244) Effects of Secondhand Smoke on Cardiovascular and Pulmonary Disease Mechanisms (R01), the proposed research is directed to the following hypothesis-based Specific Aims: 1) to examine the impact of childhood SHS exposure on longitudinal C-V risk variables profile from childhood to adulthood in black versus white nonsmoking cohorts. The C-V risk variables include obesity measures, glucose, insulin, lipids and blood pressure measured serially since childhood, and markers of inflammation, oxidative stress and endothelial function measured in adulthood; 2) to determine the independent effect of childhood SHS and its joint effect with C-V risk variables on adult subclinical C-V structure/function changes in black versus white nonsmokers. The subclinical C- V structure/function measures include carotid artery intima-media thickness, aorta-femoral pulse wave velocity, arterial wall compliance, and left ventricular geometric remodeling and function; 3) to determine the joint effect of childhood SHS and birth weight on longitudinal C-V risk variables profile from childhood and adult subclinical C-V structure/function changes in black versus white nonsmokers. The above specific aims will be examined using a longitudinal cohort followed since childhood in the Bogalusa Heart Study, a long-term biracial (black-white) community-based epidemiologic study of C-V disease beginning in childhood since 1973. The proposed study cohort consists of 800 white and 800 black adults, aged 29-52 years, who already have data on C-V risk factor variables measured serially 6 times from childhood and birth weight in the entire cohort and adulthood subclinical C-V structure/function measures on 50% of the cohort. The findings from the proposed research will provide further insights into the potential underlying mechanisms of C-V disease and help in the implementation strategies of primordial prevention in early life.